Gastro-duodenal erosive and ulcer lesions are most frequently ascribed to Н.рylori and long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs). Continuous NSAIDs therapy aimed at preventing complications of cardio-vascular diseases can cause gastroduodenal ulceration. NSAID-induced peptic ulcers are diagnosed in 20–25 % of patients, while erosions are found in over 50 %.
The erosive effect of NSAIDs on the gastro-duodenal mucosa is attributed to the inhibition of cyclooxygenase (COX), which in the presence of molecular oxygen acts as a catalyst of the key arachidonic acid pathways, cyclooxygenase and lipooxygenase. The generally believed mechanism of peptic ulceration is prevalence of aggression factors over defense factors of the mucosa, the ratio of leukotriene B4 (LTB4) and prostaglandin Е2 (PGE2) playing an important role here. Interacting with sites of COX-1 binding, NSAIDs inhibit cyclooxygenase pathway of arachidonic acid, thereby disturbing the synthesis of PGE2 which stimulates mucosal defense functions. On the contrary, LTB4 is an anti-inflammatory mediator which under certain conditions has ulcerogenic effect. The total of 70 patients with erosive and ulcer damage of the gastro-duodenal area were examined, including 39 patients with Н.рylori-associated and Н.рylori-non-associated ulcers (Group 1) and 31 patients with ischemic heart disease and erosive and ulcer lesions stemming from long-term use of the standard dose (75 mg) of acetylsalicylic acid (Group 2).
All the patients underwent common clinical examinations, laboratory tests, fibrogastroduodenoscopy (EGD), H.рylori stool antigen test, endogenous PGЕ2 and LTB4 blood tests.
According to EGD data for Group 1, gastro-duodenal mucosal hyperemia was observed in 100 % of the patients; gastric erosive and ulcer lesions were found in 7 patients (18,0 %) and duodenal ones in 21 patients (53,8 %); combined gastro-duodenal defects were diagnosed in 11 patients (28,2 %). Н.рylori was detected in 22 persons in this group (68,75%).
In Group 2 patients on NSAIDs, EGD revealed peptic mucosal hyperemia in 93 % cases; gastric erosive and ulcer lesions were diagnosed in 15 patients (48,4 %) and duodenal erosive and ulcer lesions in 5 patients (16,1 %); the combined damage was detected in 11 cases (35,5 %). 9 patients (29,0 %) were diagnosed with Н.рylori.
For classical peptic ulcers with mucosal defects localized in the duodenum, in 82 % of cases PGE2 levels exceeded 2000 pg/mL, the mean value being 2401,67 ± 58,40 pg/mL, which is apparently lower than the control values.
In Group 2 patients taking NSAIDs to prevent cardio-vascular complications, the gastric localization of erosive and ulcer defects was mainly observed. It was in this group that in 84 % of cases PGE2 levels were lower than 2000 pg/mL, the mean value being 1529,68 ± 97,84 pg/mL.
No considerable variation of LTB4 levels was observed in the experimental patients in comparison with the control group.
Despite the minor variation of LTB4 concentration in both groups, the damaging effect of leukotriene B4 against the background of diminished protective effect of prostaglandin E2 should be taken into consideration. The disturbed ratio between LTB4 and PGE2 can be a probable pathogenic mechanism of erosive and ulcer defects.
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